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May 8, 2026European Stroke Journal0 citationsOpen Access

Abstract Number: Esoc2026a2360 Case Series: Liver Cirrhosis Is a Precipitating Factor for Intracerebral Haemorrhage

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JAJemima AtputharatnamHNHlaing NiJSJulian Schwartze

Key Points

  • To report cases of intracerebral haemorrhage in patients with liver cirrhosis and explore associated management challenges.
  • Case series of 2 patients with liver cirrhosis presenting with intracerebral haemorrhage at a UK hospital in 2025.
  • Utilized the ABC approach for hyperacute management and corrected deranged INRs when necessary.
  • Patients were assessed with CT and MRI, ruling out other potential causes for ICH.
  • Patient 1 (46F) presented with right-sided paralysis and had a large left frontoparietal ICH; discharge mRS was 4, showing recovery.
  • Patient 2 (67M) presented with a moderate subcortical ICH and developed fatal status epilepticus despite no haematoma expansion.
  • Both cases underscore the complexity of managing ICH in patients with liver cirrhosis, warranting multidisciplinary approaches.

Abstract

Abstract Background and aims Intracerebral haemorrhage (ICH) incidence is elevated in patients with liver cirrhosis (LC). Mechanisms include coagulopathy and suspected microvascular dysfunction likely persisting beyond correction of haemostatic abnormalities. We report 2 patients presenting with ICH and underlying LC. Methods Our study includes 2 patients admitted to the ED of a large UK District General Hospital in 2025. Hyperacute management followed the ABC approach and deranged INRs (1 patient with thrombocytopenia) were managed with IV VITK (+ PCC for 1 patient). Patients did not require neurosurgical intervention and were transferred to the HASU. Results A 46F (mRS0) with EtOH-related LC presented following a collapse with right-sided paralysis and sensory loss. CT imaging demonstrated a large left frontoparietal ICH with intraventricular extension and no underlying small vessel disease (SVD)/neurovascular malformation (NVM). INR normalised and serial MRI/MRA imaging demonstrated absence of haematoma expansion and no microhaemorrhages, space-occupying lesion, or NVM. Discharge mRS was 4 and the patient continues to recover. A 67M (mRS3) with LC, EtOH excess and treated hypertension presented with a GCS 11/15 and right-sided paralysis. CT imaging revealed a moderate subcortical left parietal ICH, mild periventricular SVD and no NVM. The patient sadly developed fatal non-resolving status epilepticus in absence of haematoma expansion or other structural brain causes. Conclusions Both cases highlight that (i) ICH with underlying LC requires complex MDT-driven management, (ii) LC screening should be considered in patients with no convincing precipitating ICH causes and (iii) further studies are required to investigate possible cerebral microvessel dysfunction/instability in patients with LC. Conflict of interest Dr Jemima Atputharatnam: nothing to disclose, Dr Hlaing Ni: nothing to disclose, Dr Julian Schwartze: nothing to disclose

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Cite This Study

Atputharatnam et al. (2026) studied this question.

synapsesocial.com/papers/69fd8021bfa21ec5bbf087d5https://doi.org/10.1093/esj/aakag023.1804
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